Induction of DNA damage, alteration of DNA repair and transcriptional activation by stress hormones

Flint, Melanie S.; Baum, Andrew; Chambers, William H.; Jenkins, Frank J.

doi:10.1016/j.psyneuen.2007.02.013

Cited by 189 publications

(179 citation statements)

References 38 publications

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“…Actually, DNA breakage detected in the comet assay is mainly caused by mutagen-induced DNA damage [29]. These results suggest that adrenaline induces DNA damage in human lymphocytes which is consistent with the fi ndings of Flint et al [13] that stress hormones, including adrenaline, induced DNA damage in murine 3T3 cell in the comet assay. Miura et al [16] also indicated on the genotoxic potential of adrenaline.…”

Section: Discussionsupporting

confidence: 89%

“…Besides, the mutagenic potentials of adrenaline and dopamine have been reported in tests for gene mutations in L5178Y mouse lymphoma cells [12]. More recent studies revealed that adrenaline, noradrenaline and cortisol induce DNA damage in the comet assay on 3T3 cells [13]. However, adrenaline did not induce chromosome aberrations in cultured human lymphocytes [14].…”

Section: Introductionmentioning

confidence: 99%

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The Investigation of DNA Damage Induced by Adrenaline in Human Lymphocytes in Vitro/Ispitivanja Oštećenja DNK Izazvanih Adrenalinom U Limfocitima Čoveka in Vitro

et al. 2014

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Adrenaline is a neurotransmitter and hormone that plays an important role in physiological regulatory mechanisms. The objective of this study was to assess primary DNA damage in isolated human lymphocytes exposed to adrenaline using the in vitro comet assay. Dose-response of human lymphocytes was determined at concentration range of adrenaline from 0.01 μM to 300 μM for various treatment times (1h, 2h, 4h and 24h). The obtained results showed that adrenaline induced DNA damage at concentration range from 5 μM to 300 μM after 1h, 2h and 4h of treatment. The slightest DNA damage was observed after 24 h of adrenaline treatment -only the highest concentrations of adrenaline (150 μM and 300 μM) caused increased level of DNA damage. In order to evaluate the potential contribution of reactive oxygen species (ROS) in adrenaline-induced DNA damage we used antioxidants catalase (100 IU/mL and 500 IU/mL) and quercetin (100 μM and 500 μM). Co-treatment of lymphocytes with adrenaline (300 μM) and antioxidants for 1 h, signifi cantly reduced the quantity of DNA in the comet tails. Therefore, it can be concluded that adrenaline exhibits genotoxic effects mainly through induction of reactive oxygen species and that some of the DNA damage is repaired during the fi rst four hours following the treatment with adrenaline.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

The Investigation of DNA Damage Induced by Adrenaline in Human Lymphocytes in Vitro/Ispitivanja Oštećenja DNK Izazvanih Adrenalinom U Limfocitima Čoveka in Vitro

et al. 2014

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“…In the present work, the exposure of zebrafish follicles at stages I and II revealed that both stress hormones, Cort and ACTH, induced a significant increase in the tail moments in both oocyte stages, which is indicative of increased DNA damage. In accordance to our data, Cort and catcholamines induced DNA damage in the fibroblast murine cell line (3T3) (Flint et al 2007). Despite some studies relating the comet assay with apoptosis (Chiang et al 2010), the alkaline comet assay cannot elucidate which type of DNA damage is occurring, single-strand or double-strand breaks (Choucroun et al 2001, Roser et al 2001, Collins 2004.…”

Section: Discussionsupporting

confidence: 78%

Morphological and molecular effects of cortisol and ACTH on zebrafish stage I and II follicles

et al. 2015

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Oogenesis in zebrafish (Danio rerio) is controlled by the hypothalamus-pituitary-gonadal axis and reproductive hormones. In addition, an interference of stress hormones is known with reproductive biology. In the presented work, we aimed to explore the hypothesis that cortisol (Cort) and ACTH may affect early oogenesis in zebrafish, given the presence of the specific receptors for glucocorticoids and ACTH in the zebrafish ovary. Follicles at stages I and II were exposed in vitro to 1 mM Cort and ACTH for 48 h, then ultrastructural and molecular effects were analyzed. The comet assay demonstrated increased tail moments for Cort and ACTH treatment indicative of DNA damage. The mRNA expression of apoptotic genes (bax, bcl-2) was not altered by both treatments, but Cort increased significantly the expression of the ACTH receptor (mc2r). Cort stimulated the presence of the endoplasmic reticulum, predominantly at stage II, while ACTH induced a strong vacuolization. Viability of oocytes was not affected by both treatments and fluorescent staining (monodansylcadaverine/acridine orange) indicated a reduced quantity of autophagosomes for ACTH, and lower presence of nucleic acids in ooplasm for Cort and ACTH. Concluding, different responses were observed for stress hormones on early stages of zebrafish oocytes, which suggest a role for both hormones in the stress-mediated adverse effects on female gametogenesis. Reproduction (2015) 150 429-436

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“…ATM is a well-known PI3KK activated by DNA damage such as DNA doublestrand breaks, which phosphorylates several target proteins associated with the DNA damage response (Marechal and Zou 2013). GC is one of the stress hormones that induces DNA damage (Flint et al 2007;Lupien et al 2007;Flint and Bovbjerg 2012;Reeder et al 2015). The induced DNA damage could activate ATM kinase and phosphorylate UPF1 in the presence of GC, consequently enhancing GMD efficiency.…”

Section: Discussionmentioning

confidence: 99%

Identification and molecular characterization of cellular factors required for glucocorticoid receptor-mediated mRNA decay

Park

et al. 2016

Genes Dev.

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Glucocorticoid (GC) receptor (GR) has been shown recently to bind a subset of mRNAs and elicit rapid mRNA degradation. However, the molecular details of GR-mediated mRNA decay (GMD) remain unclear. Here, we demonstrate that GMD triggers rapid degradation of target mRNAs in a translation-independent and exon junction complexindependent manner, confirming that GMD is mechanistically distinct from nonsense-mediated mRNA decay (NMD). Efficient GMD requires PNRC2 (proline-rich nuclear receptor coregulatory protein 2) binding, helicase ability, and ATM-mediated phosphorylation of UPF1 (upstream frameshift 1). We also identify two GMD-specific factors: an RNA-binding protein, YBX1 (Y-box-binding protein 1), and an endoribonuclease, HRSP12 (heat-responsive protein 12). In particular, using HRSP12 variants, which are known to disrupt trimerization of HRSP12, we show that HRSP12 plays an essential role in the formation of a functionally active GMD complex. Moreover, we determine the hierarchical recruitment of GMD factors to target mRNAs. Finally, our genome-wide analysis shows that GMD targets a variety of transcripts, implicating roles in a wide range of cellular processes, including immune responses.

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Induction of DNA damage, alteration of DNA repair and transcriptional activation by stress hormones

Cited by 189 publications

References 38 publications

The Investigation of DNA Damage Induced by Adrenaline in Human Lymphocytes in Vitro/Ispitivanja Oštećenja DNK Izazvanih Adrenalinom U Limfocitima Čoveka in Vitro

The Investigation of DNA Damage Induced by Adrenaline in Human Lymphocytes in Vitro/Ispitivanja Oštećenja DNK Izazvanih Adrenalinom U Limfocitima Čoveka in Vitro

Morphological and molecular effects of cortisol and ACTH on zebrafish stage I and II follicles

Identification and molecular characterization of cellular factors required for glucocorticoid receptor-mediated mRNA decay

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